Sunday, November 11, 2012

The ECG in Figure 1 was obtained from a patient who walked into the
ED (Emergency Department) with new-onset
chest pain.

Should the cath lab be activated for acute STEMI?

If so – what do you suspect the “culprit artery” is likely to be?

How many ECG signs support your impression?

Figure 1: ECG from a patient with chest pain. What are the findings of concern? (Reproduced fromECG-2014-ePub). NOTE – Enlarge by clicking on Figures – Right-Click to open in a separate window.

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INTERPRETATION:The ECG in Figure
1 is shows normal sinus rhythm. All intervals and the axis are normal.
There is no chamber enlargement. There are however, a series of alarming
findings that were recognized by the emergency team. Emergency cardiac
catheterization was performed within 15 minutes after the patient walked into
the ED ― with successful reperfusion of a 100% proximal LAD (Left Anterior
Descending) coronary artery occlusion.

Clues to the need for
immediate catheterization and clues indicating localization of the
“culprit artery” to the proximal LAD include the following:

HyperacuteT waves in multiple leads. These are
best seen in leads aVL, V2,V3,V4.

DeWinterTwave complexes ― in which there is 1- to 3-mm of upsloping
J-point ST depression in one or more precordial leads that continue into tall,
positive symmetrical T waves (DeWinter – NEJM 359:2071, 2008). Although seen in
Figure 1 to some extent in all precordial leads except for V1 ― the
DeWinter T wave is best manifested in leads V3,V4.

IncompleteRBBB (rSr’ in lead V1; narrow terminal S waves in leads I and V6).

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DeWinter TWaves: A Sign of Proximal LAD Occlusion:

Awareness of the relatively uncommon but
highly characteristic DeWinter T wave sign is essential for not overlooking the
approximate 2% of acute anterior infarction patients who present with this ECG
manifestation (Ref 1). Rather than frank ST elevation that usually accompanies
acute LAD occlusion ― there is instead the unique DeWinter complex with
upsloping J-point ST depression blending into tall upright hyperacute T waves
in a number of precordial leads (esp.
leads V3,V4 inFigure 1). We emphasize the following key points
about this syndrome.

In patients presenting with new-onset
chest pain ― there is extremely high specificity for the DeWinter T
wave pattern and acute proximal LAD occlusion.

Rather than evolution of tall, peaked (hyperacute) T waves into frank ST segment elevation ― the DeWinter
T wave pattern was surprisingly static
over the next few hours in the DeWinter series of patients.

None of the patients in the DeWinter series who
manifested this ST-T wave pattern had acute left main occlusion on
catheterization.

Despite prompt recognition and intervention ― a
significant percentage of patients developed positive cardiac markers for acute
infarction. One ECG sign that infarction may have already occurred islossofanterior r wave amplitude (as
is seen inFigure 1).

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TAKE-HOMEPOINT:Prompt recognition of the DeWinter T wave sign in patients with new-onset chest pain with immediate
mobilization of the interventional cardiology team On-Call is essential for
minimizing the extent of acute anterior infarction.

As is the case for Wellens’ Syndrome (See Section 10.54 of the pdf in the References below) ― precordial DeWinter T waves is another unique ECG sign with
high correlation to acute anatomic coronary occlusion with mandate for
immediate intervention.

==========================================FINALPEARLS:

In addition to precordial
DeWinter T waves and loss of anterior R wave amplitude between V1-to-V2 ― there
are several additional ECG signs in Figure 1 suggestive/consistent with acute proximal LAD
occlusion. These include:

Significant ST segment elevation in leads aVR and V1.

Incomplete RBBB (that is
presumably new).

Marked reciprocal inferior ST depression.

Hyperacute T wave in lead aVL.

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ACKNOWLEDGMENT: My appreciation goes to Andrew Bowman for allowing me to use this ECG and this clinical case.

2 comments:

hello doctoris the ST depression in inferior leads due to reciprocal changes in anterior leads or is it reciprocal of the slight st elevation in AVL ? even if in AVL the STE is not egregious its existance may also give another proof of involvement of the proximal LAD .the other clue is the amount of qrs amplitude in V3 wich is very "tiny" if we compare it to the Tall T wave, isn't that highly suggestive that some ischemia is going on ?merci beaucoup

Salut Lot Ben! Good question you ask. Leads III and aVL are almost directly opposite each other - so they often show a mirror-image picture of ST elevation in one lead and ST depression in the other. If you FLIP OVER (in your mind's eye) the picture of ST elevation we see in lead III - the "mirror-image" of this would be the same shape for the ST segment in lead aVL - so I do think there IS inferior reciprocal ST depression. That said - given the cylindrical shape of the LV - any lead area can in theory be opposite any other lead area. Thus you can see "reciprocal changes" in any other lead area away from the acute of acute ongoing infarction.

ST elevation in Lead aVL is often seen with anterior MI. The picture here I think is very typical for DeWinter T waves given the dramatically tall T wave (esp in lead V3 given small height of the QRS) with J-point ST depression in V4-V6 before forming the tall T waves - so to me, highly suggestive of a proximal LAD lesion. You may want to review the 3 links I give above under References for more on these entities. THANKS again for your comment!